Sequence B appears to have more evidence to support it than Sequence A in humans. Unlike Sequence A, one of the alkaloid metabolites in Sequence B is proven to occur in humans. Some of the alkaloid metabolites theoretically created by Sequence A have only been found in some animals so far.

Please note that steps 1-3 are proven to occur for some allylbenzenes such as methyl eugenol. Step 4 is a proven alkaloid metabolite for methyl chavicol (see the article 4-Methoxycinnamoylglycine for more details). These sequences will lead to similar alkaloids as produced in Sequence A. In Sequence A the step before alkaloid creation is a ketone. Ketones tend not to form adducts as easily as aldehydes. Because step 3 is an aldehyde in Sequence B, this greatly increases the likelihood of alkaloids forming in vivo. Many aldehydes such as cinnamaldehyde are proven to form adducts with amino acids and other amines very easily without the need for a catalyst. See the article Cinnamaldehyde for more details on aldehyde adducts.

For activation Sequence B, it's important to inhibit the 1'-hydroxylation pathway. This is theorized to be a route to inactivation. Enzymes known to cause 1'-hydroxylation include CYP1A2, CYP2A6, and CYP2C9.

A proposed alternate glycine adduct is {(Z)-[(2E)-3-(3,4,5-trimethoxyphenyl)prop-2-en-1-ylidene]amino}acetic acid. Cinnamaldehyde is known to create a similar adduct with potassium glycine. See the Cinnamaldehyde article for more details.